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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5573_Библиотеки_им_академика_М_И_Перельмана.pdf
5 Acute Respiratory Distress Syndrome
109
be still indicated in patients with ventilator dyssynchrony or based on clinician
judgment and should not be automatically discounted because of ROSE.
The current recommendation is to use NMBAs within 48hours of severe ARDS
(conditional recommendation, low certainty) if oxygenation or ventilation cannot
be achieved using light sedation [3, 76]. The preferred NMBA is cisatracurium [40,
69], as it undergoes Hofmann elimination in the plasma and, therefore, does not
depend on hepatic or renal metabolism, making this ideal for ICU patients who
already have or are at risk for multiorgan dysfunction. Furthermore, its half-life of
less than 30minutes allows paralysis to be rapidly reversed.
Because NMBAs work only on voluntary skeletal muscles and have no sedative
or analgesic effects, it is imperative to concomitantly administer heavy sedation and
analgesia; otherwise, patients will have partial or full awareness while paralyzed. To
minimize such discomfort, the common practice is to sedate patients until they
reach a Richmond Agitation Sedation Scale (RASS) of −5, dened as comatose,
prior to initiation of the NMBA.
5.11 Corticosteroids
Glucocorticoids inhibit the production of pro-inammatory cytokines responsible
for driving ARDS.Their role in the treatment of ARDS has been extensively studied, and the recommendation for their use has uctuated over time. Earlier recommendation against routine use of corticosteroids for ARDS was based on a landmark
randomized, controlled trial demonstrating no mortality benet of methylprednisolone (single dose of 2mg/kg followed by 0.5mg/kg q6hours × 14days, then 0.5mg/
kg q12hours × 7 days, then tapering) in patients with ARDS of at least 7days’
duration [84]. As such, the use of corticosteroids in ARDS was limited to patients
with concomitant steroid-responsive processes such as septic shock [5, 83, 87],
Pneumocystis jirovecii infection [30], and adrenal insufciency [52].
Recently, however, the landscape has shifted in favor of using steroids to treat
ARDS.During the COVID-19 pandemic, dexamethasone (6mg qday × 10days)
was shown to signicantly improve outcomes in hospitalized patients with
COVID-19 pneumonia requiring oxygen support, including those with moderateto- severe ARDS [77, 86]. Around the same time, dexamethasone (20mg daily ×
5days, then 10mg daily × 5days) was also shown to signicantly improve mortality in moderate-to-severe non-COVID ARDS (P/F < 200) without a signal for
adverse effects such as hyperglycemia or neuromuscular weakness [89]. Moreover,
hydrocortisone (continuous infusion of 200mg per day × 4 or 7days, then tapered
for a total of 8 or 14 days) has been shown to reduce mortality in severe communityacquired pneumonia [21]. Currently, the American Thoracic Society recommends
the use of corticosteroids in patients within the rst 14days of ARDS [76] while
acknowledging some limitations to this recommendation. Initiating steroid treatment more than 14days after ARDS onset, however, may be associated with higher
mortality [53, 84]. Given the variability of clinical trials, there is no real consensus
110
L. Chen and B. D. Kraft
on which corticosteroid, dose, or duration is optimal. Moreover, the use of corticosteroids in non-intubated patients with non-COVID ARDS has not been studied.
5.12 Inhaled Pulmonary Vasodilators
The lung is the only organ in the human body that vasoconstricts in response to
hypoxia. This highly intentional physiologic response serves to maximize capillary
perfusion of only those alveolar units that participate in gas exchange. In ARDS,
however, alveolar-capillary injury is widespread leading to shunt and hypoxic pulmonary vasoconstriction. Inhaled pulmonary vasodilators, such as inhaled nitric
oxide (iNO) and epoprostenol, can be delivered exogenously to severely hypoxemic
patients and offer the theoretical benet of selectively vasodilating preserved
alveolar- capillary units to maximize gas exchange and reduce shunt fraction and
hypoxemia [78]. However, despite the physiologic improvement associated with
inhaled pulmonary vasodilators, there is no accompanying improvement in hard
outcomes such as survival [39, 44, 47]. These inhaled drugs are also used to reduce
right ventricular afterload in the setting of cor pulmonale, an unfortunate yet common complication in severe ARDS (~25% incidence) that is associated with a high
mortality [42].
5.13 Veno-Venous Extracorporeal Membrane Oxygenation
In cases of severe ARDS where it is not possible to provide tidal volumes and airway pressures within safe limits, and hypoxemia and hypercapnia are refractory to
proning and other adjunctive salvage therapies, extracorporeal life support (ECLS)
may be a rescue strategy. Veno-venous extracorporeal membrane oxygenation (VV
ECMO) diverts blood from the central venous circulation into an external device
whereby O
right heart [59]. VV ECMO can be used to support patients for days to weeks (or
longer) waiting for lung recovery. VV ECMO requires trained personnel across
multiple disciplines and is performed only at select medical centers.
The CESAR trial published in 2009 provided some of the initial evidence supporting the use of VV ECMO in patients with severe ARDS, demonstrating a mortality benet in the intervention group—those patients that were randomized to
transfer to an ECMO center (not to VV ECMO, itself) [70]. The study had numerous limitations including the lack of a standardized mechanical ventilation strategy
and its randomization to an ECMO-capable center rather than to ECMO itself
(where only 76% of subjects randomized to the ECMO center actually received
ECMO). The study was also performed prior to the widespread use of prone positioning. Nevertheless, CESAR led to signicantly increased adoption of VV ECMO
for refractory ARDS.In an effort to address some of these shortcomings, the EOLIA
and CO2 exchange occurs and oxygenated blood is returned back to the
2
5 Acute Respiratory Distress Syndrome
111
trial published in 2018 randomized subjects with very severe ARDS (P/F <50 for
3hours or <80 for 6hours, or pH <7.25 and PaCO2 ≥60mmHg for 6hours) to continued mechanical ventilation (control) or immediate VV ECMO cannulation (intervention) [19]. While EOLIA demonstrated no mortality benet of VV ECMO
compared to continued mechanical ventilation, 28% of the control group crossed
over to the VV ECMO group due to refractory hypoxemia (57% of whom died).
Subsequent post hoc analysis of EOLIA found a probable reduction in mortality by
VV ECMO [41], and a meta-analysis also concluded that VV ECMO is associated
with a reduction in mortality [58]. As a result, VV ECMO is recommended in
selected patients with severe ARDS (conditional recommendation, low evidence) [76].
Given its resource intensity and risk of life-threatening complications, patient
selection for VV ECMO should be deliberate with a focus on those patients with the
highest likelihood of lung recovery. Patients who benet most from VV ECMO are
those under 50years of age, in early-phase ARDS (≤7days), with reversible lung
injury, and with single-organ dysfunction [80, 88]. Triggers for initiation are based
commonly on EOLIA criteria assuming that the patient has failed to respond to
optimization of mechanical ventilation and other salvage therapies such as higher
PEEP, proning, and steroids [19, 70, 76].
Anticoagulation is generally initiated at the time of cannula insertion and may be
continued for the duration of VV ECMO support to prevent clot formation within
the oxygenator and circuit. However, it is not mandatory, and some centers do not
routinely anticoagulate VV ECMO circuits at all. When used, the most common
anticoagulant is unfractionated heparin (UFH), targeting an anti-Xa level of 0.3–0.5
or an activated partial thromboplastin time (aPTT) of 50–70seconds [45]; however,
the exact target ranges may vary clinically and by institution. In the case of documented or suspected heparin-induced thrombocytopenia, the preferred alternatives
are the direct thrombin inhibitors argatroban [35] or bivalirudin [82] which are noninferior to UFH.The use of anticoagulation and the development of circuit-induced
von Willebrand syndrome or thrombocytopenia make bleeding, including intracranial hemorrhage, an unfortunate but recognized complication [19, 45, 58, 59].
Unlike anticoagulation, there is no recommendation for the use of sedation or
analgesia, and its dosages are titrated based on patient needs. In early severe ARDS,
deep sedation and even paralysis of patients on VV ECMO may be required to
maintain low tidal volumes and airway pressures (see above). In the recovery phase,
however, VV ECMO can be well tolerated in a fully awake patient. In fact, early
mobilization with physical therapy, including in patients with femoral ECMO cannulation sites, is both safe and feasible [1, 13] and may improve functional independence at the time of hospital discharge [27].
Important changes in pharmacokinetics can occur when peripheral blood is circulated through a VV ECMO circuit. The addition of an extracorporeal circuit in
general increases the volume of distribution and decreases the plasma concentration
of hydrophilic drugs [81]. In addition, increased volume dilutes plasma proteins and
increases free plasma concentrations of drugs that are otherwise albumin bound
[26]. Meanwhile, lipophilic and protein-bound drugs tend to be sequestered in the
112
L. Chen and B. D. Kraft
circuit [81]. The effects of these pharmacokinetic alterations can lead to higher dosage requirements of sedation and analgesic agents and subtherapeutic plasma concentrations of antimicrobials [26].
5.14 Survivorship
Mortality from ARDS in the current era is estimated between 35% and 46% depending on the severity [8]. As a result of advances in critical care (low tidal volume
ventilation, spontaneous awakening trials, improved management of sepsis), ARDS
survival has increased over time [29]. With improved survivorship comes the
increasingly recognized phenomenon of post-intensive care syndrome (PICS), an
acquired or worsened state of cognitive, psychiatric, and/or physical dysfunction
that persists for months to years in survivors of critical illness [33].
Prevalence of cognitive impairment and psychiatric disorders following ARDS
have been reported to be 55% and 62%, respectively [56], with up to 40% of patients
scoring similarly to patients with moderate traumatic brain injury and 26% to those
with mild dementia [64]. The most commonly reported psychiatric diagnoses following critical illness survival are depression, anxiety, and post-traumatic stress
disorder [10, 56]. Cognitive impairment is signicantly associated with comorbid
psychiatric symptoms [56].
Prolonged impairment in both lung function and muscle weakness has been
widely described in survivors of ARDS.Restrictive ventilatory defects and impaired
gas exchange are reported up to a year following the index event [28, 62]. Sixminute walk distances are also shortened though improve over time [68]. Persistent
muscle weakness is associated with increased mortality at 5years [24]. The cumulative effects of these physiologic derangements are reduced independence in activities of daily living and reduced quality of life [10, 33, 56].
Risk factors for PICS include the presence of preexisting comorbidities, baseline
disability, severity of acute illness, blood glucose <100mg/dl, longer duration of
mechanical ventilation or ICU length of stay, presence of delirium, and prolonged
exposure to sedatives, among others [10, 33, 56, 79]. While preexisting conditions
are not modiable, potentially modiable variables such as sedation holidays, early
mobilization, and more liberal glycemic control may reduce the likelihood or severity of long-term neuropsychiatric and physical dysfunction.
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